Sleep homeostasis, in which the drive to sleep is a function of prior waking with sleep drive progressively increasing as waking time increases and sleep drive dissipating during sleep, controls the timing and duration of sleep in concert with circadian (time of day) input. Sleep homeostasis, or homeostatic sleep need, is often indexed by Slow Wave Activity (SWA), a 0.5-4.5 Hz oscillation in the electroencephalogram (EEG), since SWA power, as quantified by a Fast Fourier Transform of the EEG, increases with prolonged waking and decreases within sleep. Furthermore, SWA power is a better correlated to previous time awake than SWS duration and is more sensitive to sleep loss than overall sleep time or duration. Recently, we have characterized three sleep need parameters in control and genetically modified mice, including SWA power across states, SWS consolidation, and SWA decay, a new parameter that describes the dynamic expression of SWA within SWS bouts. Data from genetically modified mice indicate a critical role for adenosine, which has previously been linked to sleep homeostasis, with A1 receptor knockout mice showing fragmented sleep and an absence of SWA decay within SWS under baseline undisturbed conditions and a loss of rebound SWA following sleep deprivation, and adenosine kinase knockdown animals, in which the enzyme that converts adenosine to AMP is reduced resulting in greater adenosine levels, showing increased SWA power during both SWS and waking, more consolidated sleep, and slowed SWA decay within SWS under baseline undisturbed conditions. Additionally, further increases in SWA power and sleep consolidation in response to sleep deprivation in adenosine kinase knockdown animals. Interestingly, these changes in SWA are independent of overall SWS time. It is unknown whether these changes in homeostatic sleep need have consequences with respect to cognitive function. SWA is modified by prior waking experience and has been hypothesized to provide a mechanism by which sleep can influence learning and memory. The current proposal will use an inducible adenosine kinase knockdown model, along with a diet-based method of decreasing adenosine kinase, to investigate the effects of increased sleep need in the presence (ketogenic diet-induced adenosine kinase knockdown) and absence (inducible adenosine kinase knockdown) of overall sleep time changes on cognitive function. Y maze reversal and spatial object recognition will be used to measure prefrontal cortex and hippocampal-dependent learning and memory, respectively. The ability of increases in adenosine via SD or decreased adenosine kinase to alter cognitive function will be measured at four discrete points: acquisition, consolidation, acquisition of reversal (Y maze only), and retrieval. Furthermore, two adenosine receptor mutants (lacking A1 or lacking A2a receptors) will also be used to further investigate the effect of Ado action on sleep need. We expect that global increases in SWA acting through A1 receptors will result in learning and memory impairments irrespective of whether overall sleep time is changed.